COVID-19, caused by the SARS-CoV-2 virus, is primarily a respiratory illness, but it affects multiple body systems. Gout is a form of inflammatory arthritis resulting from the deposition of monosodium urate crystals in the joints, a condition triggered by elevated levels of uric acid in the blood (hyperuricemia). Emerging clinical evidence strongly suggests a connection between having a COVID-19 infection and the onset or exacerbation of painful gout flares. Understanding this link requires examining the body’s response to the virus and the effects of common medical treatments used during the illness.
Establishing the Link Between Viral Illness and Gout
Clinical observations and case studies have established a clear correlation between COVID-19 infection and the sudden onset of acute gout flares. This phenomenon is not unique to SARS-CoV-2, as any major viral or bacterial infection that causes severe systemic stress can trigger gout in susceptible individuals. The body’s concentrated response to severe illness acts as a potent stressor that disrupts the delicate balance of uric acid metabolism.
Studies have documented a significant rise in the rate of gout attacks during the pandemic, with one clinic reporting up to a nine-fold increase in flares compared to pre-pandemic levels. Furthermore, among patients hospitalized specifically for COVID-19, nearly one in five who had a prior history of gout experienced a flare during their hospital stay. This observed increase in attacks is closely associated with higher serum uric acid levels, confirming that the inflammatory environment created by the infection directly contributes to hyperuricemia.
Physiological Changes That Trigger Uric Acid Spikes
The body’s natural defense mechanisms against the SARS-CoV-2 virus can directly lead to the accumulation of uric acid, setting the stage for a gout flare. A primary driver is the intense systemic inflammation, often referred to as a “cytokine storm” in severe cases, which dramatically increases the rate of cellular turnover. As immune cells fight the virus and damaged cells break down, they release purines, which are then metabolized by the liver into uric acid. This excessive production overwhelms the body’s normal disposal systems.
The kidneys, responsible for excreting the majority of uric acid, are also frequently stressed during a severe COVID-19 infection. The virus can cause temporary impairment, known as COVID-19-associated nephritis, by damaging the proximal tubular cells that regulate urate transport. This injury reduces the kidney’s ability to efficiently filter and excrete uric acid, causing it to build up in the bloodstream. Metabolic stress from the illness, such as dehydration, further concentrates the uric acid, pushing levels past the saturation point necessary for crystal formation.
How Common COVID-19 Medications Affect Uric Acid Levels
Beyond the virus’s direct effects, certain medications commonly used to manage COVID-19 can inadvertently contribute to hyperuricemia. Corticosteroids, such as Dexamethasone, are widely used to temper the severe inflammatory response in hospitalized patients. While these drugs primarily act as powerful anti-inflammatories, their effect on uric acid metabolism is complex. They may initially increase urate excretion, but they can also raise uric acid levels by elevating the activity of xanthine oxidase, the enzyme that produces uric acid.
Diuretics are often administered to critically ill COVID-19 patients to manage fluid retention or pulmonary edema. Loop diuretics, like Furosemide, are known to increase serum uric acid levels by reducing its excretion via the kidneys. They compete for common transport pathways in the renal tubules, effectively blocking the removal of uric acid. Additionally, the volume depletion caused by diuretics can enhance the reabsorption of uric acid in the kidney, leading to a higher concentration in the blood and significantly increasing the risk of a gout flare.
Treatment and Prevention Strategies for Post-COVID Gout
For individuals experiencing a gout flare during or shortly after a COVID-19 infection, prompt treatment is important for managing pain and inflammation. Standard acute treatments include non-steroidal anti-inflammatory drugs (NSAIDs) and colchicine. However, it is essential to consult a physician, as the use of NSAIDs may be limited by potential kidney issues related to the COVID-19 illness, and colchicine can have complex drug interactions with some antiviral or supportive treatments.
Long-term management focuses on maintaining consistently low uric acid levels to prevent crystal formation. Patients already on urate-lowering therapies, such as allopurinol, should continue their medication to prevent a rebound flare. Lifestyle modifications are also encouraged, including maintaining adequate hydration to help the kidneys flush out uric acid and avoiding excessive consumption of purine-rich foods and alcohol. For those with multiple flares, a physician may recommend initiating long-term uric acid-lowering treatment to stabilize levels and reduce the overall burden of disease.